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Am J Physiol Heart Circ Physiol (May 8, 2003). doi:10.1152/ajpheart.01141.2002
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Submitted on December 27, 2002
Accepted on May 2, 2003

Cardiac myofibroblasts isolated from the site myocardial infarction express endothelin de novo

Laxmansa C Katwa*

* To whom correspondence should be addressed. E-mail: KatwaL{at}mail.ecu.edu.

Recently it has been demonstrated that treatment with a nonselective endothelin (ET) receptor antagonist significantly reduced myocardial infarct size, suggesting a major role for ET in tissue repair following myocardial infarction (MI). Tissue repair and remodeling found at the site of MI is mainly due to myofibroblasts (myoFb), which are phenotypically transformed fibroblasts expressing{alpha}-smooth muscle actin. It is unclear whether myoFb generate ET peptides and consequentially regulate their pathophysiological functions de novo through expression of ET1 precursor (prepro-ET1), a metalloprotease, endothelin-converting enzyme (ECE-1) required to convert big-ET1 to ET1 and ET-receptors. To address these intriguing questions, we used cultured myoFb isolated from 4 wk old MI scar tissue. In cultured cells, we found: a) expression of mRNA for ET precursor gene (ppET1), ECE, ETA and ETB receptors by semiquantitative RT-PCR (reverse transcriptase-polymerase chain reaction); b) a phosphoramidon-sensitive ECE activity, which converts big- ET1 to biologically active peptide ET1; c) expression of ETA and ETB receptors; d) elaboration of big-ET1 and ET1 peptides in myoFb culture media; and also, e) up-regulation of type I collagen gene expression and synthesis by ET, which was blocked by bosentan (an ETA and ETB receptor blocker). These studies clearly indicated that myoFb express and generate ET1 and receptor mediated modulation of type I collagen expression by ET1. Locally generated ET1 may contribute to tissue repair of the infarcted heart in an autocrine/paracrine manner.




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